中国病理生理杂志2013，Vol.29Issue(7)：1230-1234,5.DOI:10.3969/j.issn.1000-4718.2013.07.015
IL-1β通过加重脂质诱导的内质网应激导致人系膜细胞损伤
IL-1β induces human mesangial cell injury via exacerbating lipid-induced endoplasmic reticulum stress
摘要
Abstract
AIM:To investigate the molecular mechanism that interleukin-1 beta (IL-1β) exacerbates lipidinduced endoplasmic reticulum stress (ERS) and the injury of human mesangial cells (HMCs).METHODS:HMCs were cultured and divided into control group,low-density lipoprotein (LDL) group,IL-1β + LDL group and 4-phenyl butyric acid (4-PBA) + IL-1β + LDL group.Oil red O staining was used to evaluate the accumulation of lipid droplet in the cells.The mRNA levels of glucose-regulated protein 78 (GRF78),protein kinase R-like endoplasmic reticulum kinase (PERK)and α-smooth muscle actin (α-SMA) were examined by real-time PCR.Immunocytochemistry was used to observe GRP78expression.The protein level of NF-κB p65 was measured by Western blotting.The releases of IL-6 and TGF-β1 in the culture supernatants of HMCs were detected by ELISA.RESULTS:Compared with LDL group,the intracellular lipid accumulation,the mRNA levels of GRP78 and PERK,the protein expression of GRP78 and NF-κB p65,and the release of IL-6 were significantly increased in IL-1β + LDL group.Dramatically reduced intracellular lipid accumulation,down-regulated GRP78 and PERK mRNA expression,decreased protein levels of GRP78 and NF-κB p65,and suppressed IL-6 release were observed in 4-PBA + IL-1β + LDL group as compared with IL-1β + LDL group.The mRNA level of α-SMA was higher in IL-1β + LDL group than that in LDL group,and that in 4-PBA + IL-1β + LDL group was significantly depressed.CONCLUSION:IL-1β exacerbates lipid-induced ERS,thus promoting the injury of HMCs.关键词
炎症/系膜细胞/脂质沉积/内质网应激Key words
Inflammation/ Mesangial cells/ Lipid accumulation/ Endoplasmic reticulum stress分类
医药卫生引用本文复制引用
施静,崔晶晶,阳海平,刘玮,万俊丽,王志铁,邱桂霞,李秋..IL-1β通过加重脂质诱导的内质网应激导致人系膜细胞损伤[J].中国病理生理杂志,2013,29(7):1230-1234,5.基金项目
国家自然科学基金资助项目(No.81270802) （No.81270802）
国家自然科学基金青年科学基金资助项目(No.81200520) （No.81200520）
